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The ischemia of CAD can lead to serious heart damage. Acute ischemia can cause heart muscle to die, thereby weakening the heart and reducing its efficiency. Acute ischemia can also initiate a fatal arrhythmia and sudden cardiac death. Chronic ischemia, with accumulating damage from even small ischemic episodes, can lead to heart failure.
Acute Coronary Syndromes
Acute coronary syndromes are ischemic episodes caused by a sudden worsening of the atherosclerosis in coronary arteries. All acute coronary syndromes should be evaluated in an emergency department.
The acute coronary syndromes fill a spectrum from self-limiting ischemic episodes that cause little muscle death to myocardial infarctions, which cause areas of heart muscle necrosis.
Some myocardial infarctions threaten so much heart damage that the patient may need immediate reperfusion therapy. The need for immediate reperfusion is best diagnosed in a prepared emergency department that is attached to a cardiac reperfusion facility.
Always send patients with acute chest discomfort to an ED!
Health practitioners frequently receive telephone calls from patients or family members, friends, or caregivers who are concerned that their symptoms could be due to a heart attack.
Rather than dismiss such symptoms over the telephone, healthcare providers, EMS dispatchers, and staff positioned to receive these calls should advise patients to come in for an evaluation and testing. Only through a full physical examination, ECG, and appropriate blood tests to measure cardiac biomarkers can the correct diagnosis be made and appropriate interventions be given (Andersen et al., 2007).
During the last 25 years, the management of patients with acute MI has undergone many transformations. Until 1984, treatment was limited to providing symptomatic relief plus management of complications such as arrhythmias, acute heart failure, or post infarction angina. In the 1980s, the introduction of antithrombotic treatment with aspirin and intravenous (or intracoronary) fibrinolysis resulted in significant mortality reductions in patients with STEMI. In the 1990s, clinicians in some settings introduced immediate (pre-hospital) initiation of thrombolytic treatment following pre-hospital triage of patients with an acute MI and an indication for reperfusion therapy (Nauta et al., 2011).
Although more effective thrombolytic agents became available, reperfusion of the infarcted vessel often failed and bleeding complications were a limiting factor. Gradually, mechanical percutaneous techniques improved, and in the last two decades PCI became the treatment of choice in patients presenting with a STEMI (Nauta et al., 2011).
In the same time period, patients with NSTEMI benefitted from improved antithrombotic and anticoagulant therapy, better risk stratification, and tailored treatment with selective coronary revascularization in high-risk patients. In addition, effective secondary prevention was introduced with aspirin, beta blockers, statins, and ACE inhibitors in subjects with left ventricular dysfunction and, subsequently, in high-risk MI survivors. In combination, all these developments reshaped the treatment map of the patient with an MI (Nauta et al., 2011).
While they are being evaluated, patients who may have unstable angina or NSTEMI must have their ECGs monitored continuously. They also need to be near emergency resuscitation equipment including a defibrillator, because sudden cardiac death is possible (Andersen et al., 2007). These patients are usually given antiplatelet/anticoagulation therapy (aspirin, clopidogrel or prasugrel with or without heparin), oxygen when needed, nitroglycerin, additional pain relief (eg, morphine), beta blockers, and bed rest (Becker et al., 2008; Hirsh et al., 2008; Bashore et al., 2009; Smith, 2012). Coronary angiography within 24 hours is recommended for some unstable angina or NSTEMI patients.
The 2012 NSTEMI guidelines from the American Heart Association and the American College of Cardiology Foundation recommend the antiplatelet drug ticagrelor as an alternative to prasugrel and clopidogrel. Ticagrelor “significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke compared with clopidogrel, although ticagrelor was associated with a higher risk of bleeding” (Smith, 2012).
When an acute coronary syndrome is accompanied by elevated cardiac biomarkers and elevations in the ST-segment of the ECG waveform, the event is called an ST-elevation myocardial infarction (STEMI). STEMIs are myocardial infarctions that affect large areas of heart muscle and that cause transmural ischemia resulting in decreased oxygenation through the entire thickness of the heart wall. Patients with STEMIs should be identified early in the chest pain triage, because they are candidates for immediate reperfusion therapy.
The two types of acute reperfusion therapy are percutaneous coronary intervention and IV fibrinolysis. In general, percutaneous interventions are more effective than fibrinolytic therapy. However, if there is no catheter laboratory capable of performing percutaneous coronary intervention, “the appropriate and timely use of some form of reperfusion therapy is likely more important than the choice of therapy” (Levine, 2012).
Speed is important. For percutaneous coronary interventions, the time goal is to have the obstructed artery recanalized in less than 90 minutes after the patient has come into the ED. For thrombolysis, the time goal is to have injected fibrinolytic agents no later than 30 minutes after the patient has come into the ED.
The most commonly used fibrinolytic agents are reteplase, alteplase, and tenecteplase. Giving these drugs quickly is critical because they are most effective when used on new clots. Intravenous injections of a fibrinolytic agent achieve the best results when administered within 1 to 2 hours of the onset of symptoms. The benefit of this therapy decreases markedly 6 hours after symptom onset and there is hardly any benefit from thrombolytics after 12 hours (AHRQ, 2012).
Fibrinolytic therapy has the risk of inducing bleeding. Intracranial bleeding is a serious complication that occurs in about 1% to 2% of cases (AHRQ, 2012).
Percutaneous coronary intervention, often with stenting, is performed emergently in patients having a STEMI. Thrombolytics are also used for STEMIs when PCI is not available.
According to the 2013 American Heart Association STEMI guidelines, PCI is the best treatment for patients having a STEMI if it can be performed in a timely manner and by experienced clinicians. Previous guidelines recommended “door-to-balloon time” or “door-to-needle time” of 90 minutes or less. This means that a patient who qualifies for PCI should have a cardiac catheterization within 90 minutes of arrival to the ED (Husten, 2012).
The 2013 guidelines now recommend “first medical contact (FMC) to device time” of 120 minutes or less (Levine, 2012). Many EMS providers have the ability to pre-notify a hospital with a cardiac catheter laboratory by sending the ECG electronically to the ED. If the ECG is identified as a STEMI or new left bundle branch block (LBBB) by the ED diagnostician, the catheter laboratory is then notified to be ready for a procedure. Upon arrival, the patient is quickly prepped in the ED and sent for PCI. The goal is to get the patient to angiography as soon as possible because, with every moment without oxygen, more heart muscle dies.
Research suggests that most patients with LBBB do not have an occluded artery at cardiac catheterization and are therefore needlessly exposed to the risks of fibrinolytic therapy (NIH, 2016a).
The 2013 American Heart Association STEMI guidelines stress the importance of therapeutic hypothermia for unconscious cardiac-arrest survivors. During cardiac arrest, the brain is deprived of oxygen with resulting irreversible brain damage. If blood flow is restored, cerebral edema caused by tissue injury or blood–brain barrier disruption can cause even more brain damage. It has been found that these patients are likely to have a better neurologic outcome if mild hypothermia is induced.
For out-of-hospital cardiac arrest caused by ventricular fibrillation, the American Heart Association class I recommendation is induction of hypothermia to temperatures of 32°C to 34°C for a period of 12 to 24 hours in an unconscious patient who has had return of spontaneous circulation (ROSC). Hypothermia induction is a class IIB recommendation for other cases of cardiac arrest, with ROSC in an unconscious patient occurring both in and out of the hospital (Erb & Hravnak, 2012).
Coronary Artery Bypass Graft (CABG)
In a recent study sponsored by the National Heart Lung and Blood Institute, PCI outcomes were compared to cardiac bypass in diabetic patients. There was a substantial advantage of coronary artery bypass grafting (CABG) over PCI in diabetics with coronary artery disease (JournalWatch, 2012).
A new study supported by the National Institutes of Health (NIH) found older adults with stable coronary heart disease who underwent bypass surgery had better long-term survival rates than those who underwent PCI to improve blood flow to the heart muscle. While there were no survival differences between the two groups after one year, after four years the CABG group had a 21% lower mortality rate (NHLBI, 2016g).
- Consists of three intramuscular injections of tissue plasminogen activator.
- Is most effective when given >3 hours after the MI to avoid excess bleeding.
- Carries a 1% to 2% risk of inducing serious bleeding, such as intracranial hemorrhages.
- Uses a percutaneous, balloon-tipped catheter to redilate clogged coronary arteries.
Sudden Cardiac Arrest
Each year as many as 400,000 Americans die unexpectedly from an acute cardiac event. Typically, these sudden cardiac deaths (SCD) are due to a lethal arrhythmia, such as ventricular fibrillation. The risk of sudden cardiac arrest (SCA) increases with age or a history of underlying heart disease. Men are 2 to 3 times more likely to have SCA than women (NHLBI, 2016c).
Scar tissue replaces dead heart muscle cells after a heart attack. The scar tissue can disrupt and damage the heart’s electrical system and cause the electrical signals to spread abnormally throughout the heart. These changes to the heart increase the risk of dangerous arrhythmias and SCA (NHLBI, 2016c).
An acute coronary syndrome seems to cause most cases of SCA in adults. Many of these adults, however, have no signs or symptoms of CAD before having SCA. The highest risk for SCA is during the first 6 months after a heart attack (NHLBI, 2016c).
Approximately 65% of deaths caused by MI occur in the first hour. Sudden cardiac death can strike a person without previous heart symptoms, but 80% to 90% of the victims of sudden cardiac death are found to have significant stenosis of at least one major branch of the coronary arteries (Schoen & Mitchell, 2009; Zafari, 2013).
Ischemic Heart Failure
A heart is in failure when it cannot pump sufficient blood to oxygenate the body. Coronary artery disease causes heart failure through myocardial infarctions. A patient can have a single infarction that injures a large region of heart muscle, or there can be a series of small infarctions that cumulatively injure a significant amount of heart muscle.
The ischemic heart failure produced by CAD is characterized by a dilated, hypertrophic left ventricle and by scars and fibrosis in the heart muscle. Ischemic heart failure is the most common form of congestive heart failure, and it accounts for about half of all the hearts that are replaced by transplants (Schoen & Mitchell, 2009).
Heart failure increases the oxygen requirements of the heart. Medicines are prescribed based on how severe the heart failure is, the type of heart failure, and the patient response to medications (NHLBI, 2016h). Patients with both CAD and heart failure are usually given an angiotensin-converting enzyme (ACE) inhibitor, a diuretic, and digoxin. Together, these drugs reduce the size, the wall tension, and the oxygen demands of the heart. If the ACE inhibitor does not reduce ongoing hypertension, a diuretic is added (Rosendorff et al., 2007). Occasionally, beta blockers can be given, but calcium channel blockers are contraindicated.
- Diuretics (water or fluid pills) help reduce fluid buildup in the lungs and swelling in feet and ankles.
- ACE inhibitors lower blood pressure and reduce strain on the heart. They may also reduce the risk of a future heart attack.
- Aldosterone antagonists trigger the body to get rid of salt and water through urine. This lowers the volume of blood that the heart must pump, decreasing the work load of the heart.
- Angiotensin-receptor blockers relax blood vessels and lower blood pressure to decrease the heart’s workload.
- Beta blockers slow the heart rate and lower blood pressure to decrease the heart’s workload.
- Isosorbide dinitrate/hydralazine hydrochloride helps relax blood vessels so the heart does not work as hard to pump blood.
- Digoxin makes the heart beat stronger and pump more blood. (NHLBI, 2016h)
Patients with both CAD and heart failure have a relatively poor prognosis. Even when the CAD takes the form of stable angina, reperfusion therapies are considered in an attempt to improve the oxygenation of a failing heart (Antman et al., 2008).